Abstract
Renewed interest in post-injury resuscitation with hypertonic saline is due to its immunomodulatory effects. Hypertonicity reduces proinflammatory chemokine production, cell surface adhesion molecule expression, and markers of lung injury. The Tumor Necrosis Factor alpha (TNα) induced Nuclear Factor kappa B (NF-κB) pathway is a primary mediator of these proinflammatory processes. We therefore hypothesized that hypertonicity inhibits TNFα-induced phosphorylation of Inhibitor of kappa B (IκB) and activation of NF-κB.
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